{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T20:52:25Z","timestamp":1778187145587,"version":"3.51.4"},"reference-count":31,"publisher":"S. Karger AG","issue":"3-4","license":[{"start":{"date-parts":[[2020,11,20]],"date-time":"2020-11-20T00:00:00Z","timestamp":1605830400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2020,11,20]],"date-time":"2020-11-20T00:00:00Z","timestamp":1605830400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pharmacology"],"published-print":{"date-parts":[[2021]]},"abstract":"<jats:p>&lt;b&gt;&lt;i&gt;Background:&lt;\/i&gt;&lt;\/b&gt; Targeting inflammation in patients with coronary artery disease and\/or acute myocardial infarction (AMI) is a matter of debate. Methotrexate (MTX) is one of the most widely used immunosuppressants. Cardiovascular Inflammation Reduction Trial (CIRT) recently failed to demonstrate reduced cardiovascular events in MTX-treated patients. However, it is not known if long-term MTX treatment improves cardiac outcome in AMI. Therefore, in this study, we investigated the postischemic phase in MTX-treated mice undergoing AMI. &lt;b&gt;&lt;i&gt;Methods:&lt;\/i&gt;&lt;\/b&gt; Wild-type mice received MTX medication intraperitoneally for 2 weeks. Afterward, AMI was induced by transient left anterior ascending artery ligation. Postischemic cardiac damage after 24 h was assessed. &lt;b&gt;&lt;i&gt;Results:&lt;\/i&gt;&lt;\/b&gt; MTX treatment did not affect infarct size as compared to control (IS\/AAR: Con 76.20% \u00b1 12.37%\/AAR vs. MTX 73.51 \u00b1 11.72%\/AAR, &lt;i&gt;p&lt;\/i&gt; = 0.64). Moreover, systolic function and structural parameters did not differ between groups (&lt;sub&gt;24h&lt;\/sub&gt;ejection fraction: Con 36.49 \u00b1 3.23% vs. MTX 32.77 \u00b1 2.29%, &lt;i&gt;p&lt;\/i&gt; = 0.41; &lt;sub&gt;24h&lt;\/sub&gt;LVID; d: Con 3.57 \u00b1 0.17 mm vs. MTX 3.19 \u00b1 0.13 mm, &lt;i&gt;p&lt;\/i&gt; = 0.14). Platelets were increased by MTX (Con 1,442 \u00b1 69.20 \u00d7 10&lt;sup&gt;3&lt;\/sup&gt;\/mm&lt;sup&gt;3&lt;\/sup&gt; vs. MTX 1,920 \u00b1 68.68 \u00d7 10&lt;sup&gt;3&lt;\/sup&gt;\/mm&lt;sup&gt;3&lt;\/sup&gt;, &lt;i&gt;p&lt;\/i&gt; &amp;#x3c; 0.0001). White blood cell and RBC as well as rate of monocytes, granulocytes, lymphocytes, and serum amyloid P levels were equal. &lt;b&gt;&lt;i&gt;Conclusion:&lt;\/i&gt;&lt;\/b&gt; MTX medication did not improve postischemic cardiac damage in a murine model of AMI. Future trials are needed to identify and investigate other anti-inflammatory targets to improve cardiovascular outcome. <\/jats:p>","DOI":"10.1159\/000511279","type":"journal-article","created":{"date-parts":[[2020,11,20]],"date-time":"2020-11-20T22:00:54Z","timestamp":1605909654000},"page":"225-232","source":"Crossref","is-referenced-by-count":8,"title":["MTX Treatment Does Not Improve Outcome in Mice with 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